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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone. Aldosterone excretion, however, was extremely low. Alkaluria, high urinary sodium excretion and hypercalciuria were observed. The patient admitted to chronic ingestion of large amounts of baking soda. Upon cessation of alkali abuse, his blood pressure fell dramatically; orthostatic hypotension, concomitant azotemia, hemoconcentration, hyperkalemia and weight loss occurred. Despite dramatic elevation in plasma renin activity, urinary aldosterone excretion remained low during this period. Adrenal glucocorticoid secretion was intact. All abnormalities of sodium, potassium and aldosterone subsequently returned to normal. A 10 day challenge with oral sodium bicarbonate was associated with a rise in blood pressure, but serum calcium remained normal. The patient remains normotensive 15 months after discontinuing alkali abuse.
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PMID:Hypertension corrected by discontinuing chronic sodium bicarbonate ingestion. Subsequent transient hypoaldosteronism. 111 72

Morphological studies of the parathyroid glands from adult Mongolian gerbils in which hypercalcaemia had been induced by thyroidectomy and calcium injections for 2-19 days were carried out. The potassium pyro-antimonate technique and subsequent X-ray analysis of the precipitates were used for ultrastructural localization of cations. Ultrastructurally, most (suppressed) chief cells exhibited a dense cytoplasm, medium-sized or large mitochondria, glycogen particles, inconspicuous endoplasmic reticulum and Golgi complex, calcium-containing precipitates mainly in mitochondria and nuclei, and sometimes also lysosomal bodies and accumulations of secretory granules which occasionally seemed to be discharged into cytoplasmic vacuoles. A few parenchymal cells showed a low cytoplasmic density, few organelles, and structurally altered mitochondria, occasionally with associated smooth-surfaced vacuoles. These cells possessed calcium-containing precipitates in mitochondria, smooth-surfaced vacuoles, and also diffusely in the cytosol. It is concluded, that, in the main part of the parenchymal cells, the hypercalcaemia had resulted in a suppression primarily of the synthetic and later also of the secretory activity, and that the calcium-containing precipitation is different in the chief cell variants.
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PMID:Parathyroid morphology in gerbils after thyroidectomy and calcium administration. 118 57

Diuretics act primarily by blocking reabsorption of sodium at four major sites in the nephron. Clinically useful agents that block sodium reabsorption effectively in the proximal tubule are lacking. Furosemide (Lasix), ethacrynic acid (Edecrin), and possibly organomercurial agents are effective in the ascending limb of Henle's loop. Thiazides are the major agents acting in the early distal tubule. In the late distal tubule and collecting duct, spironolactone (Aldactone) and triamterene (Dyrenium) are useful, especially in combination with diuretics which act more proximally. In treating edematous states, initial therapy with thiazides is effective in most patients who do not exhibit moderate or severe renal insufficiency, severe hyperaldosteronism with excessive distal reabsorption of sodium in exchange for potassium, or excessive sodium reabsorption in the proximal tubule or ascending limb. Nonedematous states in which diuretic therapy is useful include hypertension, hypercalcemia, hypercalciuria, diabetes insipidus, and acute renal failure.
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PMID:Diuretic agents. Mechanisms of action and clinical uses. 126 95

Six cases of acute renal failure (ARF) due to rhabdomyolysis were experienced between 1984 and 1989. Patients' ages ranged from 33 to 92 years old (average ages 61) and all were male. The causes of rhabdomyolysis were as follows: one crush syndrome, one acute arterial occlusion, one diabetic hyperosmolar nonketotic coma and three cases of malignant syndrome due to neuroleptica (mainly haloperidol). Underlying diseases included, one case of abdominal aneurysm, two cases of diabetes mellitus, two cases of schizophrenia and one case of reactive psychosis. Dehydration was considered as an important factor in the onset of rhabdomyolysis and ARF, because it was observed in 4 of the cases in this study. In all cases, the serum levels of potassium, phosphorus and uric acid as well as myoglobin and myogenic enzymes increased markedly. In patients with myoglobinuric ARF, severe metabolic acidosis and hypocalcemia in the oliguric phase and hypercalcemia in the diuretic phase were prominent. Muscle biopsy showed myolytic degeneration in 2 of 4 cases. Five cases were treated with hemodialysis and one case was managed conservatively. All 6 cases had relatively good prognosis. However, 3 cases with malignant syndrome showed outcomes more severe than in the other 3 cases without such syndrome.
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PMID:[Acute renal failure due to rhabdomyolysis--clinical investigation on our 6 cases]. 163 34

The ratio of reabsorption of osmotically free water to osmolal clearance in individual urine voids was about the same before and after short-term spaceflights (the points fall on the same regression line). This ratio was reduced after long-term flights, so that the regression lines for pre- and postflight values have different slopes. This change in the function relating the two factors was accompanied by increased vasopressin in blood plasma and probably was caused by altered cellular reaction to vasopressin. The decrease in the effect of vasopressin may have been caused by development of hypokalemia and hypercalcemia in the cosmonauts, and decrease in cellular potassium in the outer renal medulla (this effect was observed in experiments on rats after flights on biosatellites). We established that, in addition to cAMP, cGMP and inositol trisphosphate participate in cellular reactions to vasopressin. Increases in the concentration of cGMP and decrease in the formation of inositol trisphosphate in the presence of neomycin increase the hydro-osmotic effect of vasopressin. We hypothesize that modulation of the effect of vasopressin in cosmonauts is due to change in the functional state of their kidneys.
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PMID:Mechanism of postflight decline in osmotic concentration of urine in cosmonauts. 166 Feb 60

The effect of local and systemic calcium administration was tested on the pancreas of cat and guinea pig. After 3 h of local calcium infusion (0.6 mmol/kg x h) via the splenic artery of the cat hemorrhagic pancreatitis could be shown. Control animals treated with potassium (1.1 mmol/kg x h) or 0.9% NaCl alone showed no morphological change in the pancreas. Intravenous administration of calcium (0.6 mmol/kg x h) led to a 1.8-fold increase in serum ionized calcium levels in the cat and a 1.6-fold increase in levels in the guinea pig. The cat showed necrosis of acinar and ductal cells throughout the gland at 12 h. In the guinea pig, acinar cell vacuolisation and cell necrosis started at 3 h, and at 9 h degeneration of entire acini, hydropic swelling and degeneration of ductal cells, and perivascular leukocytic infiltration was present. In both species, a significant increase in the number of intraductal precipitates and a significant increase in urinary amylase output was present in calcium treated animals. The findings suggest that hypercalcemia has a deleterious effect on the pancreas that causes acinar and ductal cell necrosis and eventually pancreatitis.
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PMID:Acute hypercalcemia induces acinar cell necrosis and intraductal protein precipitates in the pancreas of cats and guinea pigs. 198 43

We evaluated the effects of an increased serum potassium level, the result of a potassium infusion, on the pressor response to infused calcium in normotensive men. Potassium infusion (0.38 mmol/kg per h for 2 h) increased serum potassium by 1.1 mmol/l with no changes in blood pressure, cardiac output or total peripheral vascular resistance (n = 6). Calcium infusion (0.19 mmol/kg per h for 1 h) and combined infusion of potassium followed by calcium increased serum calcium by 1.1 mmol/l with an elevated blood pressure, vascular resistance and no change in cardiac output (n = 8). The absolute and per cent increases in blood pressure and vascular resistance during the calcium infusion did not differ in the absence compared with in the presence of an increased serum potassium. These results indicate that a small increase in serum potassium did not modify the pressor response to infused calcium. We conclude that hypercalcaemia-induced hypertension is caused by direct effects of calcium on arterial smooth muscle.
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PMID:The failure of increased serum potassium to enhance the pressor response to infused calcium in normotensive men. 184 66

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.
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PMID:Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction. 188 51

Idiopathic hypercalciuria, defined as the urinary excretion of more than 300 mg. calcium per day in men or more than 250 mg. calcium per day in women, or more than 4 mg. calcium per kg. per day, is observed in about 50 per cent of the patients with calcium oxalate/apatite nephrolithiasis and is one of the risk factors for stone formation. These patients do not exhibit hypercalcemia, elevated serum parathyroid hormone concentrations or urinary cyclic adenosine monophosphate excretion nor clinical evidence of sarcoidosis, other granulomas or a malignancy. Hypophosphatemia may be present. Augmented rates of intestinal absorption of dietary calcium account for most of the increments in urinary calcium. Serum 1,25-dihydroxyvitamin D concentrations are in the upper normal range or elevated among many patients and are normal but not suppressed in the others. Activation of 1,25-dihydroxyvitamin D formation may be secondary to hypophosphatemia or other, as yet undefined, factors. Since, 1,25-dihydroxyvitamin D apparently can up-regulate its own receptor, small increments in its synthesis and blood levels could amplify the effect of the hormone to stimulate intestinal calcium absorption. Calcium balances are slightly but significantly negative and urinary hydroxyproline excretion may be increased so that a generalized disorder of calcium homeostasis also involving bone may be present. Additional studies are required to determine the genetic basis for the occurrence of idiopathic hypercalciuria in families, the cause of greater expression of idiopathic hypercalciuria in men and whether environmental factors (high dietary sodium chloride, protein and purified carbohydrate intakes) contribute to the expression of idiopathic hypercalciuria. Although thiazide diuretics, inorganic phosphate, magnesium hydroxide and potassium citrate have provided effective therapy, prospective studies are needed to determine optimum therapy and the optimum duration of treatment.
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PMID:Idiopathic hypercalciuria. 264 29

The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.
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PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34


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